Candida albicans is an asexual yeast species. Candida albicans is a major fungal pathogen of humans. It is can be found as a harmless commensal organism, inhabiting mucosal membranes and the digestive tract; a benign saprophyte. However, Candida albicans, can infect both internal organs and mucous membranes of the mouth, throat, and genital tract, and can cause a chronic infection; it can cause superficial infections, such as oral thrush, and can cause severe, often fatal, systemic infections, especially in immunocompromised patients.
There has been a growing number of cases of thrush and other diseases caused by Candida albicans; and, this can be attributed mainly to medical advances in antibiotic, steroid and immunosuppressive treatments, as well as to immunocompromising ailments such as HIV and AIDS. Indeed, surveillance of nosocomial blood stream infections (BSI) in the USA between April 1995 and June 1996 revealed that Candida albicans was the fourth leading cause of nosocomial BSI (Pfaller et al., “National surveillance of nosocomial blood stream infection due to Candida albicans: frequency of occurrence and antifungal susceptibility in the SCOPE Program,” Diagn Microbiol Infect Dis 1998 May;31(1):327–32). Accordingly, Candida albicans, and compositions and methods for detecting, diagnosing, preventing or treating Candida albicans are medically significant.
Thrush is characterized by creamy-white, curdlike patches on the tongue and other mucosal surfaces of the mouth. The disease is caused by an overgrowth of Candida albicans. Patients susceptible to thrush include immunocompromised individuals, e.g., adults whose immune systems have been weakened by antibiotics, steroids, immunosuppression treatments, AIDS, and the like, as well as infants, for instance if the mother had a vaginal yeast infection.
Painful, raw and bleeding areas result if the curdlike discharge is removed from patches of thrush. These superficial lesions may allow the yeast to spread to other areas of the body. Candida albicans can invade major organs, causing serious complications.
While thrush is typically treated with a topical agent, and there are oral and intravenous treatments for Candida albicans infections, chronically infected patients may require long term therapy with oral and/or intravenous therapy.
Moreover, strains of Candida albicans resistant to present treatments or therapies such as amphotericin B, fluconazole, itraconazole and other azole antifungals have been isolated (Mori et al., “Analysis by pulsed-field gel electrophoresis of Candida albicans that developed resistance during antifungal therapy,” Nippon Ishinkin Gakkai Zasshi 1998;39(4):229–33; Pfaller et al., supra; Rex et al., “A randomized trial comparing fluconazole with amphotericin B for the treatment of candidemia in patients without neutropenia,” N Engl J Med Nov 17, 1994;331(20):1325–30). Indeed, in Rex et al., in certain individuals, treatment failed to clear infection from the bloodstream, and Candida albicans was infection commonly associated with the treatment failure.
Thus, there is a need for new treatments or therapies against Candida albicans. 
Diagnosis of Candida albicans requires microscopic identification of the pseudomycelial (branching-arms) forms. There is likewise a need for new compositions and methods for diagnosing or detecting Candida albicans. 
The ESS1 gene was originally discovered in Saccharomyces cerevisiae, by inventor Hanes working in the laboratory of Dr. Peter Shank and Dr. Keith Bostian (Hanes 1988). It was discovered in a search for cell growth control genes. By gene disruption techniques, ESS1 was shown to be essential for yeast cell growth, hence the name (Essential) (Hanes et al. 1989). ESS1 genes are highly conserved. Homologs of the ESS1 gene have been found in Drosophila, humans and several other organisms. The fly gene (called dodo) and the human gene (called PIN1) encode proteins that are 45% identical to the yeast Ess1 protein (Maleszka et al. 1996; Lu et al. 1996).
U.S. Pat. No. 5,952,467 to Hunter et al. relates to the identification and characterization of Pin1, a protein of mammalian origin that associates with NIMA protein kinase. It was determined that overexpression of Pin1 activity induces a specific G2 arrest and delays NIMA-induced mitosis, while depletion of Pin1 triggers mitotic arrest and nuclear fragmentation. The specification provides for a method of controlling the growth of a cell by contacting the cell with a composition which modulates the Pin1 activity. The corresponding nucleic acid sequence encoding Pin1 is identified in U.S. Pat. No. 5,972,697 to Hunter et al.
However, prior to the present invention, the Candida albicans ESS1 or CaESS1 gene had not been isolated, or sequenced; or disclosed or suggested, nor had corresponding amino acid sequences from the gene been disclosed or suggested. Likewise, fragments or portions of the gene and protein had not been disclosed or suggested. Also, diagnostic, prophylactic, therapeutic, or similar compositions and methods involving the gene and/or the protein and/or fragments of the gene and/or fragments of the protein, had not been taught or suggested.
In view of the significance of Candida albicans, and the need for new therapies, treatments, means for prevention, and means for diagnosing or detecting Candida albicans, providing the CaESS1 gene, portions thereof, amino acid sequences from the gene, fragments or portions of the protein, and diagnostic, prophylactic, therapeutic, or similar compositions and methods involving the gene and/or the protein and/or fragments of the gene and/or fragments of the protein, are significant advances in the art, addressing problems in the art.